Uncoupling the roles of the SUV3 helicase in maintenance of mitochondrial genome stability and RNA degradation.
Yeast SUV3 is a nuclear encoded mitochondrial RNA helicase that complexes with exoribonuclease, DSS1, to function as a RNA degradosome. Inactivation of SUV3 leads to mitochondrial dysfunctions such as respiratory deficiency, accumulation of aberrant RNA species including excised group I introns, and loss of mitochondrial DNA (mtDNA). Although intron toxicity ... has long been speculated as the major reason for the observed phenotypes, direct evidence to support or refute this theory is lacking. Moreover, it remains unknown whether SUV3 plays a direct role in mtDNA maintenance independently of its degradosome activity. In this communication, we address these questions by employing an inducible knockdown system in S. cerevisiae with either normal or intronless mtDNA background. Expressing mutants defective in ATPase (K245A) or RNA binding activities (V272L, or ΔCC that carries an eight amino acids deletion at C-terminal conserved region), resulted in not only respiratory deficiencies but also loss of mtDNA under normal mtDNA background. Surprisingly, V272L, but not other mutants, can rescue the said deficiencies under intronless background. These results provide genetic evidence supporting the notion that the functional requirements of SUV3 for degradosome activity and maintenance of mtDNA stability are separable. Furthermore, V272L mutants and wild-type SUV3 associated with an active mtDNA replication origin and facilitated mtDNA replication, while K245A and ΔCC failed to support mtDNA replication. These results indicate a direct role of SUV3 in maintaining mitochondrial genome stability that is independent of intron turnover, but requires the intact ATPase activity and the CC conserved region.
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Date: Sep. 12, 2011
PubMed ID: 21911497
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